ArticleHuman molecular genetics2010
Prdm16 is required for normal palatogenesis in mice.
Article in Human molecular genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
87 citing papers in PubMed, 1 synthesis or guideline pooled it, 149 citations in OpenAlex.
- Pooled it
- A Review of PRDM13 Transcriptional Regulation in Vertebrate Retinal Development and Disease.Investigative ophthalmology & visual science · 2026Review
- Prdm16 Amplifies Notch Signaling and Suppresses Venous Lineage Specification to Prevent Arteriovenous Malformations During Vascular Development.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- PRDM paralogs are required for Meckel's cartilage formation during mandibular bone development.Developmental biology · 2026Article
- Prenatally diagnosed chromosome 1p36 deletions: a retrospective case series, literature review, and genotype-phenotype correlations.BMC medical genomics · 2025Review
- PRDM16, a new kid on the block in cardiovascular health and disease.Cardiovascular research · 2025Review
- PRDM16 functions as a co-repressor in the BMP pathway to suppress neural stem cell proliferation.eLife · 2025Article
- Kölliker's Organ Functions as a Developmental Hub in Mouse Cochlea Regulating Spiral Limbus and Tectorial Membrane Development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Article
- PRDM16 determines specification of ventricular cardiomyocytes by suppressing alternative cell fates.Life science alliance · 2024Article
- Unveiling the Spectrum of Minor Genes in Cardiomyopathies: A Narrative Review.International journal of molecular sciences · 2024Review
- Clinical and Genetic Correlation in Neurocristopathies: Bridging a Precision Medicine Gap.Journal of clinical medicine · 2024Review
- Prdm16 mutation determines sex-specific cardiac metabolism and identifies two novel cardiac metabolic regulators.Cardiovascular research · 2024Article
- PRDM16 co-operates with LHX2 to shape the human brain.Oxford open neuroscience · 2024Article
- Epigenetic regulation of craniofacial development and disease.Birth defects research · 2024Review
- Nonsense Variant PRDM16-Q187X Causes Impaired Myocardial Development and TGF-β Signaling Resulting in Noncompaction Cardiomyopathy in Humans and Mice.Circulation. Heart failure · 2023Article
- Cardiovascular Phenotypic Spectrum of 1p36 Deletion Syndrome.Journal of pediatric genetics · 2023Article
- Ezh2-dependent methylation in oral epithelia promotes secondary palatogenesis.Birth defects research · 2023Article
- PRDM16 deficiency in vascular smooth muscle cells aggravates abdominal aortic aneurysm.JCI insight · 2023Article
- Candidate genes for obstructive sleep apnea in non-syndromic children with craniofacial dysmorphisms - a narrative review.Frontiers in pediatrics · 2023Review
27 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Transcriptional cofactors are essential to the regulation of transforming growth factor beta (TGFbeta) superfamily signaling and play critical and widespread roles during embryonic development, including craniofacial development. We describe the cleft secondary palate 1 (csp1) N-ethyl-N-nitrosourea-induced mouse model of non-syndromic cleft palate (NSCP) that is caused by an intronic Prdm16 splicing mutation. Prdm16 encodes a transcriptional cofactor that regulates TGFbeta signaling, and its expression pattern is consistent with a role in palate and craniofacial development. The cleft palate (CP) appears to be the result of micrognathia and failed palate shelf elevation due to physical obstruction by the tongue, resembling human Pierre Robin sequence (PRS)-like cleft secondary palate. PRDM16 should be considered a candidate for mutation in human clefting disorders, especially NSCP and PRS-like CP.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.